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Reprinted from Coffey CE, Cummings JL (eds): The American Psychiatric Publishing Textbook of Geriatric Neuropsychiatry, Third Edition.
Used with permission. Copyright © 2011 American Psychiatric Association. www.appi.org.
10
Electroconvulsive Therapy
and Related Treatments
C. Edward Coffey, M.D.
Charles H. Kellner, M.D.
E
those with general medical comorbidity. Refinements in ECT
technique (discussed in “Technique of ECT” later in this
chapter) have largely obviated those initial concerns so that
now a large proportion of patients receiving ECT are elderly,
and this number will increase as the population continues to
age. Kramer (1985) reviewed patterns of ECT use in California from 1977 to 1983 and found that the probability of receiving ECT increased with age of the patient. Patients ages 65
years and older were given ECT at a rate of 3.86/10,000 population, compared with 0.85/10,000 in those ages 25–44 years.
In an analysis of the data on ECT use in California from 1984
to 1994, Kramer (1999) found similar patterns. Babigian and
Guttmacher (1984) reviewed a massive data set from the
Monroe County (New York) Psychiatric Case Register over
three 5-year periods. They found that among patients hospitalized for the first time, those who received ECT were older
than those who did not. Lambourn and Barrington (1986)
surveyed the use of ECT from 1972 to 1983 in a British population of 3 million and found that ECT use was more common
in patients (especially female patients) ages 60 years and older.
In a study of 5,729 psychiatric admissions over 3 years, Malla
(1988) found that patients who received ECT in general hospitals were significantly older than patients who did not receive ECT. Thompson et al. (1994) analyzed data from the National Institute of Mental Health Sample Survey program for
1980 and 1986, which included representative samples of psychiatric inpatients in the United States. They found that approximately one-third of ECT recipients were ages 65 years
and older, a figure far out of proportion to the representation
of that age group in the sample (8.2%). Rosenbach et al.
(1997) studied a sample (∼4,000 people) of Medicare Part B
claims from 1987 to 1992 and found an ECT rate of 5.1/10,000
population. In an analysis of inpatient data from the 1993
lectroconvulsive therapy (ECT) is a sophisticated medical
procedure that uses electrical stimulation applied to the scalp to
induce a series of brief, controlled seizures in a patient who is
under general anesthesia. ECT is a safe, rapidly acting, and
highly effective treatment for certain severe neuropsychiatric
disorders, most notably mood disorders (including those in patients with neurological disorders), some forms of schizophrenia, and syndromes such as delirium and catatonia (American
Psychiatric Association 2001; U.K. ECT Review Group 2003).
In this chapter, we review the use of ECT as a treatment for
neuropsychiatric disorders in elderly patients. We discuss the
indications and efficacy, medical physiology, mechanisms of
action, contemporary technique, and safety and adverse effects of this important procedure, as well as its unique role in
patients with neurological disorders. In addition, we preview
some experimental “brain stimulation” therapies that are related to ECT and that may hold promise for the future. These
therapies include focal electrically administered seizure therapy (FEAST) and magnetic seizure therapy (MST). Other
brain stimulation therapies are discussed in Chapter 11, “Brain
Stimulation Therapies: Vagus Nerve Stimulation, Transcranial
Magnetic Stimulation, Transcranial Direct Current Stimulation, and Deep Brain Stimulation.”
ECT in Geriatric
Neuropsychiatric Practice
Although precise data are not available, Hermann et al. (1995)
estimated that ∼4.9 patients per 10,000 population receive
ECT annually in the United States. For years after its introduction in 1938, ECT was used primarily in younger adults because of concerns about its safety in older patients and in
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The American Psychiatric Publishing Textbook of Geriatric Neuropsychiatry, Third Edition
Healthcare Cost and Utilization Project of the Agency for
Healthcare Policy and Research, Olfson et al. (1998) found
that ∼10% of 22,761 patients admitted to a general hospital
with a principal diagnosis of recurrent major depression received ECT that year. Increasing age was one of several patient
variables associated with higher ECT use; persons ages 65
years and older were seven times more likely to receive ECT
than were persons ages 18–34 years.
Several factors help to explain the frequent use of ECT in
elderly patients. First, elderly individuals may be more sensitive to medication side effects, particularly the combination of
antidepressants and antipsychotics typically required to treat
psychotic depression. Second, evidence suggests that antidepressant pharmacotherapy may be less effective in elderly than
in younger patients (Roose et al. 2004). In contrast, increasing
age as a variable may be a positive predictor of ECT response
(Black et al. 1993; Coryell and Zimmerman 1984; O’Connor et
al. 2001; Tew et al. 1999). Third, elderly patients are more likely
to have comorbid general medical or neurological disorders,
which may complicate the use of psychotropic medications or
limit their effectiveness (Mottram et al. 2006). For all these reasons, ECT is a critically important component of the neuropsychiatrist’s tool kit used to treat mood disorders in elderly
patients. Indeed, several studies have found that the use of ECT
is one of the most important variables associated with a positive outcome in later-life depression (Bosworth et al. 2002;
Philibert et al. 1995; Rubin et al. 1991; Zubenko et al. 1994). Finally, ECT appears to be at least as cost-effective as pharmacotherapy (Greenhalgh et al. 2005; McDonald 2006), and perhaps even more so in certain settings (Olfson et al. 1998).
Diagnostic Indications and Efficacy
ECT is indicated for the acute treatment of severe mood disorders (including depression or mania), certain forms of
schizophrenia, and syndromes such as delirium and catatonia.
ECT is also an effective form of continuation treatment for
some of these conditions (discussed later in this chapter in
“Technique of ECT”). The neurobiological effects of ECT may
also prove salutary in other neuropsychiatric syndromes, such
as Parkinson’s disease (discussed later in this chapter in “ECT
in Elderly Patients With Neurological Disorders”).
Depression
The most common indication for ECT in all patients, including those who are elderly, remains the acute and maintenance
treatment of depression, both major and bipolar. In elderly
patients with depression, ECT is typically used as a secondline treatment, after patients have failed to respond to a trial of
medication or have exhibited intolerance of the side effects of
medication. ECT should be considered a first-line intervention in certain situations, however, such as when the presenting illness threatens the patient’s life (e.g., severe suicide risk,
severe melancholia with inanition and malnutrition, inability
to comply with critical general medical care), when ECT is
deemed safer than alternative treatments, or when the patient
has a history of response to ECT or a preference for ECT (American Psychiatric Association 2001).
Six randomized controlled trials have found ECT superior
to sham ECT in adults with depression (reviewed in Abrams
2002b). A reanalysis of one of these trials (the Nottingham
trial; Gregory et al. 1985) found that the efficacy of ECT was
also superior to sham ECT in elderly patients with depression
(O’Leary et al. 1995). Although a Cochrane Review of the randomized evidence concluded that the data were too sparse to
determine the efficacy of ECT in depressed elderly patients
(Stek et al. 2003), subsequent reviews, which included the extensive nonrandomized literature, concluded that ECT is indeed effective in the acute treatment of depression in elderly
patients (Dombrovski and Mulsant 2007; Flint and Gagnon
2002; Salzman et al. 2002; Van der Wurff et al. 2003).
The reported response rates to ECT among elderly patients
with depression range from 63% to 98%, clearly demonstrating that increasing age, per se, does not have a negative impact
on the effectiveness of ECT for depressive illness. In fact, evidence suggests that ECT may be even more effective in elderly
patients than in younger age groups (O’Connor et al. 2001),
and several reports have confirmed the efficacy and safety of
ECT even in the “old-old” (the low end of which is variably defined as between ages 75 and 85) (Casey and Davis 1996; Cattan et al. 1990; Gormley et al. 1998; Manly et al. 2000).
ECT is reported to be 20%–45% more effective than pharmacotherapy for depression (see review by Abrams 2002b), as
confirmed in two meta-analyses (Janicak et al. 1985; U.K. ECT
Review Group 2003). This same therapeutic superiority of
ECT over antidepressant pharmacotherapy has also been demonstrated in elderly patients (Folkerts et al. 1997; Salzman et al.
2002). No somatic therapy for depression has been shown to
have efficacy superior to that of ECT (Sackeim 2005).
Certain clinical features may predict a particularly robust
response to ECT among patients with depression. Data derived
largely from mixed-age samples of adults suggest that a particularly good response to ECT is associated with the presence of
psychosis, catatonia, pseudodementia, pathological guilt, anhedonia, agitation, and neurovegetative signs (Greenberg and
Fink 1992; Hickie et al. 1996; Salzman 1982; Zorumski et al.
1988). These findings were confirmed in a prospective study
involving 29 elderly patients (Fraser and Glass 1980), in which
guilt, anhedonia, and agitation were identified as positive prognostic signs. In multiple studies, response to ECT has been particularly good in patients with delusional depression, com-
Reprinted from Coffey CE, Cummings JL (eds): The American Psychiatric Publishing Textbook of Geriatric Neuropsychiatry, Third Edition. Copyright © 2011 American Psychiatric Association.
Electroconvulsive Therapy and Related Treatments
pared with a nonpsychotic group (Hickie et al. 1996; Mulsant
et al. 1991; Pande et al. 1990; Petrides et al. 2001; Wilkinson et
al. 1993), although other studies have found no difference
(O’Leary et al. 1995; Rich et al. 1984a, 1986; Sobin et al. 1996;
Solan et al. 1988). Delusions are common in depressed elderly
persons, and typically these patients respond poorly to pharmacotherapy. The use of ECT in agitated or psychotic elderly
patients may spare them exposure to antipsychotic agents. This
consideration is important, given the risks of antipsychotic
drugs to induce motor (e.g., tardive dyskinesia), metabolic,
and vascular complications in elderly patients (Jenike 1985; see
also Chapter 9, “Geriatric Neuropsychopharmacology”). Suicide is a major concern for patients with depression, and the
risk of this outcome is particularly high in elderly people (especially men). ECT is rapidly effective against suicidal ideation
(Kellner et al. 2005), an advantage that is particularly important to elderly patients, who may respond more slowly to antidepressant medications than do younger patients (Mulsant et
al. 2006).
A variety of biological markers for ECT response have
been investigated in mixed-age samples, including the dexamethasone suppression test, the thyrotropin-releasing hormone test, and other neuroendocrine tests (Decina et al. 1987;
Kamil and Joffe 1991; Kirkegaard et al. 1975; Krog-Meyer et
al. 1984; Papakostas et al. 1981; Swartz 1993), as well as polysomnographic studies (Coffey et al. 1988; Grunhaus et al.
1996) and the apolipoprotein E polymorphism (Fisman et al.
2001). None of these laboratory studies appears to provide
strong “state-specific” markers for major depressive illness,
and data are inconsistent (Devanand et al. 1991) on whether
they can be used serially to follow the course of ECT, predict
outcome, or predict early relapse.
Several authors have attempted to identify predictors of
nonresponse to ECT. In a retrospective study, Magni et al.
(1988) compared elderly patients who responded to ECT and
those who did not respond and found that physical illness during the index episode, fewer negative life events preceding the
onset of the index episode, and prior depressive episodes of
long duration were predictive of nonresponse to ECT. Other
investigators have found that longer duration of the index episode predicts poorer outcome (Fraser and Glass 1980; Karlinsky and Shulman 1984). Previous courses of ECT and increased age at the time of first treatment with ECT have been
linked with a slower response rate to ECT, with no effect on
eventual positive outcome (Rich et al. 1984b; Salzman 1982;
Shapira and Lerer 1999). There are conflicting data on whether
pre-ECT medication resistance predicts nonresponse to ECT
(Rasmussen et al. 2007a), with response rates ranging from
28% to 72% depending on the patient sample, definition of
“medication resistance,” and ECT treatment protocol (Dombrovski et al. 2005). The limited data, however, should not dis-
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courage the clinician from initiating a trial of ECT in patients
with any of the aforementioned predictors of nonresponse.
The fact that patients who receive ECT come from a selected
population that is less responsive to antidepressant medication
and generally is at greater risk for relapse underscores the value
of this treatment for the most difficult-to-treat elderly patients.
Although few studies have directly compared residual depressive symptoms following ECT and following pharmacotherapy, full remission is likely to be more common following
ECT (Hamilton 1982). Residual depressive symptoms have a
serious impact on the quality of life and may result in chronicity of depression in elderly patients and increase the likelihood
of relapse (Prien and Kupfer 1986). A number of studies have
suggested that use of ECT is one of the most important variables in predicting a positive outcome of depression in elderly
patients, with reduced chronicity, decreased morbidity, and
possibly decreased mortality (Avery and Winokur 1976;
Babigian and Guttmacher 1984; Philibert et al. 1995; Wesner
and Winokur 1989; Zubenko et al. 1994).
Mania
Although extensive clinical experience indicates that ECT is
effective for treating both manic and depressed phases of bipolar illness in elderly patients, formal data for this population are lacking. A small number of controlled studies involving relatively young mixed-age samples have found ECT to be
superior to drug therapy (Mukherjee 1989; Mukherjee et al.
1988; Small et al. 1988, 1991). ECT appears to be particularly
effective in mixed bipolar states and agitated mania, conditions that may become more prevalent as the illness becomes
more chronic and refractory (Calabrese et al. 1993). ECT may
be particularly suitable for elderly patients who have this more
severe form of bipolar disorder. Also, morbidity from ECT is
likely to be less risky than the general medical risks of a sustained period of mania in an older person.
Schizophrenia and
Other Psychotic Disorders
No controlled data exist on the use of ECT in elderly patients
with schizophrenia. ECT has been used in younger patients
with this illness, and in these patients several features correlate
with good outcome, including the presence of affective or
catatonic features, an acute onset of illness with relatively brief
duration of illness, and a history of response to ECT (American Psychiatric Association 2001; Braga and Petrides 2005;
Tharyan and Adams 2005). ECT does not appear to be very effective for treating the chronic, residual phase of the illness
with predominant negative features (Weiner and Coffey
1988). These “deficit” states become more common as the illness progresses (Kaplan and Sadock 2005) and thus may be
Reprinted from Coffey CE, Cummings JL (eds): The American Psychiatric Publishing Textbook of Geriatric Neuropsychiatry, Third Edition. Copyright © 2011 American Psychiatric Association.
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The American Psychiatric Publishing Textbook of Geriatric Neuropsychiatry, Third Edition
highly represented in elderly patients with schizophrenia, although controlled data on this issue are lacking. To the best of
our knowledge, there are no systematically collected data on
the efficacy of ECT in patients with late-onset functional psychoses, such as late-onset schizophrenia.
Delirium and Catatonia
Although no controlled data have been reported on the use of
ECT in patients with delirium (see Chapter 15, “Delirium”),
numerous case and clinical series have documented its safety
and effectiveness, irrespective of the underlying etiology of the
delirium (see Krystal and Coffey 1997 for a review). Indeed,
ECT has been used for the management of neuropsychiatric
symptoms of delirium in Europe and Scandinavia for decades
(Kramp and Bolwig 1981). The use of ECT in patients with
delirium is generally reserved for those who have not responded to more standard general medical treatment (American Psychiatric Association 2001).
Catatonia is a potentially life-threatening syndrome whose
symptoms overlap with those of delirium (see Chapter 15). A
large clinical literature supports the effectiveness of ECT as a
safe and rapidly effective treatment for catatonia and related
conditions, such as neuroleptic malignant syndrome (Caroff et
al. 2007; Fink and Taylor 2003).
Medical Physiology of ECT
The data on the physiology of ECT have been compiled largely
from mixed-age adult samples, and to our knowledge, few
data focus specifically on the physiology of ECT in elderly patients. Clearly, the myriad physiological changes that accompany an ECT seizure take on particular importance in elderly
individuals, in whom general medical illnesses involving multiple organ systems are common. Of greatest importance are
the physiological effects of ECT on the brain and the cardiovascular system. As described later in this chapter, modifications in ECT technique may be required in patients with brain
or cardiovascular disease (see “Technique of ECT” and “ECT
in Elderly Patients With Neurological Disorders”).
Cerebral Physiology
With ECT, an electrical stimulus applied to the scalp is used to
depolarize cerebral neurons and thereby produce a generalized cerebral seizure. The mechanism by which ECT seizures
are propagated is not well understood. Bilateral ECT appears
to lead to seizure generalization through direct stimulation of
the diencephalon (a subcortical “pacemaker”), whereas seizures induced with unilateral stimulation may begin focally in
the stimulated cortex and then generalize via corticothalamic
pathways (Staton 1981).
During the initial phase of the induced seizure, electroencephalographic (EEG) activity is variable, consisting of patterns of low-voltage fast activity and polyspike rhythms. These
patterns correlate with tonic or irregular clonic motor movements. With seizure progression, EEG activity evolves into a
pattern of hypersynchronous polyspikes and waves that characterize the clonic motor phase. These regular patterns begin
to slow and eventually disintegrate as the seizure ends, sometimes terminating abruptly in a flat electroencephalogram for
several seconds (Weiner and Krystal 1993). The entire seizure
typically lasts 30–60 seconds, and preseizure EEG rhythms are
typically recovered within 20–30 minutes. It should be noted
that although the scalp-recorded electroencephalogram implies that the ECT seizure is an all-or-none phenomenon, in
fact the onset, duration, and EEG morphology of the seizure
all vary according to the brain structures involved. The interictal (intertreatment) electroencephalogram typically shows
mild slowing, particularly in frontal regions. These ictal and
interictal EEG features vary with ECT technique (i.e., stimulus waveform, stimulus electrode placement, stimulus dosage,
stimulus parameters, and treatment frequency and number),
as well as with the patient’s age. For example, increasing age is
associated with shorter seizure duration; shorter slow-wavephase duration; weaker overall strength and patterning; and
lower early ictal, midictal, and postictal amplitudes (Krystal et
al. 1995, 1998).
The ECT-induced seizure is also associated with a variety
of transient and benign changes in cerebral physiology (reviewed in Abrams 2002b). In patients with depression, cerebral
blood flow is typically reduced frontally at baseline, increased
during the ECT seizure, and then either increased or decreased
relative to baseline after ECT, depending in part on the timing
and measurement technique employed. The increase in cerebral blood flow during the seizure produces a brief increase in
intracranial pressure that is rarely of clinical consequence but
is the reason for extreme caution when ECT is used in patients
with space-occupying mass lesions. Studies of cerebral permeability generally confirm that the structural integrity of the
blood-brain barrier is maintained during ECT, despite the rise
in cerebral blood flow. A variety of changes in regional cerebral
glucose metabolism (measured with positron emission tomography) are reported either during or after ECT (Nobler et al.
2001), but no consistent patterns have emerged. The effects of
age on all these cerebral physiological changes have not been
described systematically, although in animals, age is associated
with increased blood-brain permeability changes after 10 electroconvulsive seizures (Oztas et al. 1990).
Cardiovascular Physiology
ECT results in a marked activation of the autonomic nervous
system, and the relative balance of parasympathetic and sympa-
Reprinted from Coffey CE, Cummings JL (eds): The American Psychiatric Publishing Textbook of Geriatric Neuropsychiatry, Third Edition. Copyright © 2011 American Psychiatric Association.
Electroconvulsive Therapy and Related Treatments
thetic nervous system activity determines the observed cardiovascular effects (Applegate 1997). Vagal (parasympathetic) tone
is increased during and immediately after administration of the
electrical stimulus, and this may be manifested by bradycardia or
even a brief period of asystole. With development of the seizure,
activation of the sympathetic nervous system occurs, resulting in
a marked increase in heart rate, blood pressure, and cardiac
workload. Peripheral stigmata of sympathetic activation, including piloerection and gooseflesh, may also be observed. The
tachycardia and hypertension continue through the ictus and
generally end along with the seizure. Near or shortly after the
end of the seizure, there may be a second period of increased vagal tone, which may be manifested by bradycardia and various
dysrhythmias, including ectopic beats. As the patient awakens
from anesthesia, there may be an additional period of increased
heart rate and blood pressure as a result of arousal and further
sympathetic outflow (Welch and Drop 1989).
The cardiovascular responses during ECT combine to
produce an increase in myocardial oxygen demand and a decrease in coronary artery diastolic filling time. Transient electrocardiographic changes in the ST and T waves are seen in
some patients during the procedure, but it is unclear whether
these findings are related to myocardial ischemia (McCall
1997; Zvara et al. 1997). An alternative mechanism may be a
direct effect of central nervous system stimulation on cardiac
repolarization (Welch and Drop 1989). No corresponding increase in levels of cardiac enzymes has been found to accompany these electrocardiographic changes (Braasch and Demaso 1980). In a study of patients receiving ECT, Messina et
al. (1992) obtained echocardiograms during and after ECT
treatments and found transient regional wall motion abnormalities more often in patients with ST-T wave changes on
electrocardiograms (ECGs), suggesting a period of demand
myocardial ischemia. The clinical importance of these findings remains to be evaluated.
The effects of age on the cardiovascular response to ECT
have been examined in only a few modern studies. Shettar et al.
(1989) randomly assigned 19 patients (mean age 51 years;
range 19–84 years) to ECT with pretreatment with glycopyrrolate or with placebo; the alternate pretreatment drug was used
for the subsequent ECT treatment (i.e., each patient served as
his or her own control). For both types of pretreatment, there
was no correlation between age and length of poststimulus
asystole. In two controlled studies of mixed-age samples that
included elderly patients (Prudic et al. 1987; Webb et al. 1990),
no relationship was found between age and ECT-induced
changes in heart rate, blood pressure, or rate-pressure product.
In a study of relatively younger patients (mean age 43 years;
range 20–64 years), Huang et al. (1989) noted a significant inverse correlation between age and increases in blood pressure
and rate-pressure product.
281
Although these results suggest that age, per se, is not associated with the extent of the cardiovascular response to ECT,
these findings must be interpreted cautiously. Some of the
subjects in these studies (especially those who were older)
were also receiving antihypertensive drug therapy that may
have attenuated their cardiovascular response to the treatments, and other clinical observations suggest that at least
some elderly patients with cardiovascular disease may be at
risk for marked increases in pulse and blood pressure during
ECT (Applegate 1997; Zielinski et al. 1993; see also “Cardiovascular Side Effects” later in this chapter).
Mechanisms of Action of ECT
Despite considerable research into the neurobiology of ECT,
its mechanism of action remains a mystery. ECT produces
both acute and long-standing changes in brain chemistry, endocrinology, physiology, and neurogenesis and neuroplasticity (Holtzmann et al. 2007; Wahlund and von Rosen 2003).
Current hypotheses of the mechanism of action of ECT focus
on the anticonvulsant effects of the treatment (Sackeim 1999)
or the extent and efficiency of seizure generalization throughout the brain and the resultant neurobiological effects in relevant brain regions (particularly prefrontal and diencephalic)
(Abrams 2002b). It remains unclear, however, whether any of
these neurobiological changes account for the clinical effects
of ECT or whether they merely represent epiphenomena.
Furthermore, the broad therapeutic spectrum of ECT (i.e., in
addition to its antidepressant properties, ECT also exhibits
antimanic, antipsychotic, anticonvulsant, and anticatatonic
effects) would seem to make it unlikely that a single mechanism of action will explain all of these effects.
Technique of ECT
Pretreatment Evaluation
When a patient is referred for ECT, a formal pretreatment
evaluation is carried out by a practitioner credentialed in ECT
to 1) determine if ECT is indicated, 2) establish baseline measures of efficacy and cognitive side effects, 3) identify and treat
any general medical conditions that may increase the risk of
adverse effects (performed in conjunction with an anesthesia
provider), 4) determine the setting (inpatient or outpatient)
in which the treatments should be administered, 5) initiate the
process of informed consent, and 6) prepare the patient and
family or significant other for the procedure (American Psychiatric Association 2001; Coffey 1998).
The indications for ECT (discussed in “Diagnostic Indications and Efficacy” earlier in this chapter) are confirmed through
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The American Psychiatric Publishing Textbook of Geriatric Neuropsychiatry, Third Edition
a thorough neuropsychiatric history and examination (see
Chapter 4, “Neuropsychiatric Assessment”). The patient’s response to previous therapies, including ECT, should be thoroughly documented. Handedness should also be assessed
because of its relevance to nondominant unilateral electrode
placement (Kellner et al. 1997). Because the hand used for writing is a fallible indicator, patients should be asked which hand
they use to throw a ball, cut with a knife, and so on (American
Psychiatric Association 2001).
The neuropsychiatric history and examination also provide an opportunity to obtain objective baseline data essential
for assessing the outcome of the course of ECT. A variety of
measures of symptom severity are available for each diagnostic indication (e.g., the Montgomery-Åsberg Depression Rating Scale or the Hamilton Rating Scale for Depression for depression, the Brief Psychiatric Rating Scale for psychosis), and
these can be used as markers of efficacy when administered
regularly over the treatment course. Both clinician- and patient-rated instruments should be considered, given the potential dissociation between observer- and self-rated symptom severity. Measurement of baseline cognitive function (in
particular, attention and memory) is essential to assess any
cognitive side effects from the course of ECT. The ideal cognitive measure would be brief, inexpensive, simple to administer, and sensitive to change in both verbal and nonverbal
spheres, and it would have multiple forms (to avoid practice
effects). Although several instruments are available, none is
ideal, and options range from a bedside mental status examination, to a brief instrument such as the Mini-Mental State
Examination, to formal neuropsychological testing.
A general medical history and examination are also performed to identify any active general medical problems, with a
focus on the brain, the cardiovascular system, the musculoskeletal system, the dentition, and the upper gastrointestinal
tract. Any personal or family history of problems with anesthesia should also be noted. A limited laboratory evaluation
(serum potassium, ECG) is sufficient for most patients, with
other studies ordered only as clinically indicated. Consultation with anesthesia specialists is important because the provision of general anesthesia is associated with some, albeit
small, medical risk. Indeed, an anesthesiologist experienced in
ECT may also serve as the “general medical” consultant and
can greatly facilitate the evaluation of patients with serious
systemic illness. Although ECT has no “absolute” contraindications, serious disease of the brain (e.g., aneurysm, tumor),
heart (ischemia or failure), or other systems (e.g., pheochromocytoma, retinal detachment) will require stabilization and
optimal treatment and may necessitate additional consultation with other specialists, such as cardiologists, neurologists,
or neurosurgeons.
Adjustments may also be required in some of the patient’s
general medications. Theophylline levels should be monitored
closely or discontinued if possible, because high blood levels
during ECT have been associated with status epilepticus (Fink
and Sackeim 1998). Metrifonate and echothiophate are organophosphate medications that irreversibly inhibit cholinesterase and pseudocholinesterase, and may cause prolonged
apnea when combined with succinylcholine and should not
be given. In theory, the duration of succinylcholine muscle relaxation could be increased by cholinesterase inhibitors such
as rivastigmine, donepezil, tacrine, and galantamine, which
are used in patients with Alzheimer’s disease (see Chapter 16,
“Alzheimer’s Disease and the Frontotemporal Dementia Syndromes”). However, case reports (Zink et al. 2002) and growing clinical experience suggest that acetylcholinesterase inhibitors may be continued safely during ECT. Otherwise, patients
should take any required medications as scheduled.
Typically, psychotropic medications are stopped before ECT,
with the exception of antipsychotics and possibly antidepressants (Farah et al. 1995). Lithium taken around the time of
ECT has been linked to an increased occurrence of delirium
and prolonged seizures (Weiner et al. 1980). For most patients,
lithium can be discontinued or at least held for 1 day before
ECT, with serum lithium levels kept as low as clinically feasible
(Dolenc and Rasmussen 2005; Kellner et al. 1991a). Complete
discontinuation of lithium may not be advisable for other patients with severe and recurrent mood disorder, particularly
when ECT is used as a continuation/maintenance treatment.
Thus, the decision to use lithium concurrent with ECT must be
made on a case-by-case basis. Benzodiazepine use should be
minimized or stopped, whenever possible, before ECT. Benzodiazepines may impair the induction or spread of the therapeutic seizure, thereby potentially decreasing treatment response (Kellner 1997b; Pettinati et al. 1986). The use of these
agents by elderly patients may also theoretically increase their
susceptibility to cognitive side effects from ECT. When necessary, the use of the lowest feasible doses of agents with relatively
short half-lives and no active metabolites (e.g., lorazepam, oxazepam) has been recommended (American Psychiatric Association 2001). Similarly, anticonvulsant medications prescribed for psychiatric indications (e.g., mood stabilizers)
should usually be tapered and discontinued before ECT, to
avoid problems with seizure induction or effectiveness. Antidepressant medications are usually stopped to avoid cumulative cardiac and central nervous system side effects, although
this practice is now being reconsidered, particularly with the
newer agents (American Psychiatric Association 2001). Studies have reported conflicting findings on whether the addition
of an antidepressant medication enhances the efficacy of ECT
(Lauritzen et al. 1996; Mayur et al. 2000; Sackeim et al. 2009;
Seager and Bird 1962).
Reprinted from Coffey CE, Cummings JL (eds): The American Psychiatric Publishing Textbook of Geriatric Neuropsychiatry, Third Edition. Copyright © 2011 American Psychiatric Association.
Electroconvulsive Therapy and Related Treatments
Initiating the informed consent process is another essential
element of the pre-ECT workup. Written informed consent
for ECT is required from any patient with the capacity to give
voluntary consent, and the consent form and process must be
in compliance with all applicable laws, statutes, and standards.
Patients who lack such a capacity may require the judicial appointment of a legal guardian to provide the consent. The
American Psychiatric Association provides a pertinent sample
of an informed consent document for ECT and discusses in
detail the appropriate process for obtaining such consent
(American Psychiatric Association 2001).
The complexities of voluntary consent for an elderly patient with a neuropsychiatric disorder are discussed in Chapter 14, “Ethical and Legal Issues.” With the increased prevalence of cognitive impairment in elderly patients, competency
to consent becomes a major issue, and the education of both
patient and family becomes essential. This is also a time in the
patient’s life cycle when children are becoming increasingly
responsible for their parents, and the patient’s children should
be involved in the consent process whenever possible. Of particular relevance to ECT, compared with younger patients,
those over age 65 appear to be less aware that they can refuse
ECT (Malcolm 1989).
Finally, the pre-ECT evaluation affords the clinician an
opportunity to establish important interpersonal relationships with the patient and family. These relationships can be
therapeutic and enhance patient satisfaction, as well as provide personal reward to the clinician.
ECT Procedure
In the United States, ECT is commonly given as a series of single treatments on alternate mornings, typically at a frequency
of three times a week (on Monday, Wednesday, and Friday).
Many patients receive the treatments on an outpatient basis,
as long as certain precautions are taken (Fink et al. 1996).
First, the patient’s psychiatric illness must allow for safe management outside the hospital. Clearly, acute suicide risk or agitated psychosis often requires hospitalization. Second, the
patient’s general medical status should be stable enough for
safe outpatient management. In addition, elderly persons are
at risk for falling, and ECT may temporarily exacerbate this
risk (Rao et al. 2008). Third, strong social support is required,
because family members or others must transport the patient
to and from the treatment facility, ensure that the patient takes
nothing by mouth for at least 8 hours before a treatment session, and provide supervision between treatments (with particular attention paid to ensuring that the patient refrains
from driving and making important financial or personal decisions while experiencing cognitive side effects) (Fink 1994).
For some patients, it is helpful to administer the first (or several initial) ECT treatment(s) on an inpatient basis and then
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switch to outpatient treatments once it has been established
that outpatient treatments can be administered safely and
comfortably.
The treatment team consists of a psychiatrist, an anesthesiologist, and specially trained nursing personnel. ECT is typically given in either a special treatment suite or the recovery
area of an operating room suite. Patients have been previously
evaluated for treatment indications and coexisting general
medical conditions by the ECT practitioner and anesthesia
provider, appropriate treatment of these conditions has been
implemented, and the consent process has been initiated. Patients should have nothing to eat or drink for at least 8 hours
before treatment. The standard technique requires the establishment of a patent intravenous line. Electrodes for stimulation and for monitoring the seizure are applied according to
appropriate technique (Kellner et al. 1997). Before anesthesia
induction, a verbal “time-out” procedure should be conducted to confirm the patient’s identity and details of the procedure (e.g., stimulus electrode placement, medication dosages). Administration of the anesthesia and maintenance of
the patient’s airway are under the direction of the anesthesia
provider. The medication sequence includes anticholinergic
premedication (glycopyrrolate or atropine) to prevent vagalmediated cardiac slowing (if indicated), followed by an anesthetic (usually methohexital) and then succinylcholine for
muscle relaxation. Throughout the procedure, the patient is
ventilated with 100% oxygen by mask, and heart rate, ECG,
blood pressure, and blood oxygen saturation are monitored.
Once the patient is asleep and thoroughly relaxed, a specially designed bite block is inserted into the patient’s mouth,
to protect the tongue and teeth from injury during jaw clenching as the electrical stimulus is applied (caused by direct electrical stimulation of the temporalis muscles). A predetermined electrical stimulus (see “Electrical Stimulus Mode,
Waveform, and Dosing” later in this chapter) is delivered
across electrodes placed on the patient’s properly prepared
scalp. Typically, a generalized seizure ensues and lasts from
30 to 60 seconds. The seizure is monitored by electroencephalography and by observation of the motor manifestations of
the seizure, typically at the right ankle where a blood pressure
cuff was inflated above systolic pressure immediately before
administration of succinylcholine (the cuff is deflated once
the seizure has ended). Ventilatory support is continued until
the patient emerges from the anesthesia, and further recovery
is provided in an environment with as little stimulation as
possible. The entire procedure takes ∼20 minutes, and patients are often able to have breakfast within 1 hour of the time
of treatment. They are discharged shortly thereafter.
A typical acute course of ECT consists of 6 to 12 treatments,
although occasionally patients may require fewer or more
treatments to achieve full response. The treatment schedule is
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often modified in elderly patients to lessen cognitive side effects, with treatments given once or twice per week rather than
three times per week (American Psychiatric Association 2001;
Freeman 1995; Kellner et al. 1992; Lerer et al. 1995). ECT is
stopped when maximal clinical improvement is thought to
have been achieved or when further improvement is not noted
between treatments. Special attention is then given to continuation/maintenance treatment with either medication or ECT.
Anesthesia Considerations
Brief, light general anesthesia is used during ECT to render the
patient unconscious during (and thus amnesic for) the procedure. Methohexital is the agent of choice because it has a rapid
onset and a brief duration of action, it induces minimal postanesthesia confusion, and it is relatively inexpensive. Methohexital also appears to have a lesser anticonvulsant effect than
thiopental or propofol (Bergsholm and Swartz 1996), which
benefits seizure induction and spread. Still, because methohexital is an anticonvulsant and because the seizure threshold
is often increased in elderly patients (see the following section), the lowest effective anesthetic dose is desirable. Because
methohexital dosing is based on lean body mass, the required
methohexital dosage in many elderly patients may be less than
1 mg/kg total body weight (Fragen and Avram 1990).
Etomidate is a reasonable alternative to methohexital, especially in cases of severe cardiovascular disease, but it is more
expensive and is associated with pain on infusion, longer cognitive recovery time, and short-term adrenocortical suppression. Ketamine may be considered in patients with high seizure
thresholds because of its proconvulsant properties, although it
is somewhat slower acting and has a longer duration of action.
Propofol, another alternative anesthetic agent, is well tolerated
but has anticonvulsant properties and may be associated with
shorter seizures (American Psychiatric Association 2001).
The preferred neuromuscular blocking agent for ECT is
succinylcholine, primarily because it has rapid onset and a
brief duration of action. The use of succinylcholine may require special consideration in elderly patients. Succinylcholine indirectly stimulates muscarinic cholinergic receptors in
the sinus node, causing a prolonged depolarization followed
by a depolarized state, which is resistant to further stimulation. The initial depolarization may contribute to bradycardia, especially if serial doses are required. This effect may be
pronounced in patients receiving beta-blockers and in those
with evidence of preexisting conduction delay, both frequently the case among elderly patients. Pretreatment with
anticholinergics, such as atropine or glycopyrrolate, will block
this bradycardic effect. Succinylcholine may also trigger lifethreatening hyperkalemia in patients who have muscle wasting, a potential concern in some elderly patients who have severe inanition from melancholia or in those who have been
relatively immobilized (e.g., from stroke or neuromuscular
disorders). Use of a nondepolarizing muscle relaxant should
be considered in these patients.
Intragastric pressure also increases with the use of succinylcholine, related to abdominal skeletal muscle fasciculation, and this may increase the risk of gastric reflux and aspiration. Certain groups of elderly patients (e.g., those with
hiatal hernia, gastroparesis, or morbid obesity) are at risk for
substantial gastroesophageal reflux during the procedure,
with subsequent risk for aspiration pneumonitis (Zibrak et al.
1988). Smokers are particularly prone to morbidity from aspiration (Lichtor 1990). In these patients, additional strategies beyond withholding oral food and fluids before a session
may be considered to decrease gastric acidity (e.g., premedication with histamine H2 receptor antagonists or sodium citrate) and volume (e.g., premedication with metoclopramide)
(Lichtor 1990).
Electrical Stimulus Mode,
Waveform, and Dosing
The ECT stimulus should be delivered with a contemporary
bidirectional, constant-current, brief-pulse device. A constant
current provides for stable delivery of the ECT stimulus over a
range of patient impedances. The brief-pulse waveform, with
a pulse width of 0.5–2 milliseconds, is a more efficient and
physiological stimulus for inducing seizures, relative to the
sine wave current (phase period ∼8.33 milliseconds) employed by early-model ECT devices, and therefore is associated with decidedly fewer cognitive side effects without loss of
efficacy. The two major ECT devices currently produced in the
United States—spECTrum by MECTA (Figure 10–1) and
Thymatron System IV by Somatics (Figure 10–2)—are designed to deliver constant-current, brief-pulse stimulation,
the use of which is strongly recommended by numerous professional organizations.
The ECT stimulus intensity, or stimulus dosage, should be
sufficiently above the patient’s seizure threshold to induce an
effective seizure. Older patients require higher ECT stimulus
intensities to elicit such seizures than do younger patients, because seizure threshold (the amount of electricity required to
elicit a seizure) increases with age, as well as with gender
(higher in males) and stimulus electrode placement (higher in
bitemporal than in unilateral nondominant) (Coffey et al.
1995a; Sackeim et al. 1991). This age effect is believed to be the
result of a decrease in the excitability of the brain but may also
be partially due to increases in skull thickness (electrical resistance) with aging. It should be noted that the efficiency of seizure induction with the brief-pulse stimulus may vary as a
function of the parameters (i.e., pulse width, frequency, duration, and current) of the stimulus set. For a given stimulus
charge, those stimuli with shorter pulse widths and longer
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FIGURE 10–1.
Frontal view of the spECTrum 5000Q ECT device by MECTA.
FIGURE 10–2.
Frontal view of the Thymatron System IV ECT device by Somatics.
train durations are more efficient at seizure induction (i.e., are
associated with a lower seizure threshold) than those with
longer pulse widths. We recommend using parameter sets that
employ pulse widths of 0.5–1 milliseconds. Research is under
way to determine the clinical effects of even shorter pulse
widths (so-called ultra-brief-pulse ECT) (Sackeim et al. 2008).
The precise stimulus dosage for optimal ECT has yet to be
determined. Data in adult mixed-age samples suggest an interaction of stimulus dosage, stimulus parameters, electrode
placement, and clinical efficacy. Bitemporal ECT is clinically
effective at a stimulus dosage of 1.5–2.5 times seizure threshold (so-called moderate-dose ECT), but optimal unilateral
nondominant ECT may require a stimulus dosage of ∼4–6
times seizure threshold (so-called high-dose ECT) to match
the efficacy of bitemporal ECT (McCall et al. 2000; Sackeim et
al. 1993, 2000, 2008). In a study of 39 elderly inpatients with
major depression, Stoppe et al. (2006) found similar rates of
remission in those randomly assigned to high-dose unilateral
nondominant ECT (88% remission) and in those who received moderate-dose bitemporal ECT (68% response rate).
Thus, a critical factor in the efficacy of ECT appears to be the
stimulus dosage relative to the patient’s seizure threshold, adjusted for the effects of stimulus electrode placement.
The ECT specialist may use a number of options to determine the proper stimulus dosage for an individual patient
(Coffey 2008). One approach is to employ a stimulus titration
procedure at the first treatment to estimate initial seizure
threshold and then adjust stimulus dosage upward accordingly at subsequent treatments (Coffey et al. 1995a). However,
with this maneuver the first treatment can be assumed to be
less than optimally effective if unilateral nondominant electrode placement is employed (because the seizure will be elicited by a “barely suprathreshold” stimulus dosage known to
be subtherapeutic), and it carries a small risk of bradycardia
and asystole associated with stimulation of the parasympathetic nervous system. These problems are obviated by an alternate “fixed-dose” method wherein the initial stimulus dose
is set at 75%–100% of the maximum output (∼576 mC) of
contemporary U.S. ECT devices for right unilateral electrode
placement or at approximately half the patient’s age (in per-
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centage of device output) for bilateral electrode placement
(Petrides and Fink 1996). That dosage could then be titrated
upward or downward at subsequent ECT treatments, using
some established physiological “benchmark” of an “effective”
seizure, such as peak heart rate or quantitative EEG metrics
(e.g., percentage adequacy, postictal suppression index).
Seizure threshold increases during ECT (the well-known
anticonvulsant effect), at times necessitating increases in stimulus dose during the course of therapy (Coffey et al. 1990,
1995b; Kellner et al. 1997). This effect does not appear to be
more pronounced in elderly patients, but because this population has a higher initial seizure threshold, some older patients
may eventually require stimulus intensities during their course
of treatment that exceed the maximal dosage of the ECT device
(Krystal et al. 2000; Lisanby et al. 1996). In this setting, successful seizure induction may be accomplished with the use of
more efficient stimulus parameter sets (as discussed above) or
by a switch to a proconvulsant anesthetic agent such as ketamine.
Stimulus Electrode Placement
ECT is generally administered through stimulus electrodes
placed bitemporally, bifrontally, or in a unilateral nondominant position (the right side for most patients). The choice of
stimulus electrode placement is complex. Studies in mixed-age
samples of adults suggest that right unilateral ECT has fewer
cognitive side effects, but as noted above, unless stimulus dosage and electrode application are carefully prescribed and certain medications restricted, treatment efficacy may be limited
with this placement. Bilateral (bitemporal) electrode placement may be more reliably effective but may be associated with
greater cognitive side effects (for a review, see Abrams 2002b).
Few studies have addressed the issue of electrode placement specifically in elderly patients. In a meta-analysis of the
early literature, Pettinati et al. (1986) found a trend for improved efficacy in elderly patients receiving bilateral treatment.
In one of the few controlled studies, Fraser and Glass (1980) assigned 29 elderly patients with depression to either unilateral
or bilateral ECT two times a week. Stimulus-dosing strategies
were unclear. No group differences were observed in terms of
therapeutic response or memory performance after ECT, but
those subjects randomly assigned to bilateral electrode placement required more time to become reoriented after the fifth
ECT treatment. More recently, Stoppe et al. (2006) randomly
assigned 39 elderly inpatients to unilateral or bitemporal highdose ECT and found similar remission rates (88% and 68%, respectively) but fewer cognitive side effects with unilateral ECT.
No studies have examined whether the effects of cerebral disease or age-related structural brain changes modify the therapeutic or adverse effects of unilateral versus bilateral ECT in
elderly patients.
Thus, limited data exist to guide the choice of ECT electrode placement in elderly patients with neuropsychiatric illness. A reasonable approach in most elderly patients is to begin
with unilateral nondominant ECT at a sufficiently high stimulus dosage; if minimal or no response is seen by the fifth or sixth
treatment, then switch to bilateral ECT at moderate stimulus
dosage. Because bilateral ECT may be associated with a statistically greater likelihood of response, it may be considered the
treatment of choice in patients in urgent need of care. If intolerable cognitive side effects develop with bilateral ECT, the
treatment may be changed to unilateral ECT once the affective
disorder has begun to respond (other techniques for lessening
cognitive side effects are discussed later in this chapter in “Adverse Effects of ECT and Their Management”). Finally, atypical
electrode placements (e.g., left unilateral, right frontotemporal–left frontal, or bifrontal) may be clinically useful in some
elderly patients (Bailine et al. 2000; Kellner 1997a, 2000; Little
et al. 2004).
Seizure Monitoring
The ECT seizure should be monitored to confirm that a seizure
has occurred and to determine when it has ended (Kellner et al.
1997; Weiner and Krystal 1993). The seizure may be monitored indirectly by observation of the motor response (convulsion) of a “cuffed” extremity, but additional monitoring with
ictal electroencephalogram is now considered the standard of
care. The ictal electroencephalogram has been studied using
sophisticated computer analysis to determine whether seizure
“potency” (and treatment efficacy) may be predicted by various indices such as amplitude, regularity, or coherence (Krystal
et al. 1995, 1996; Weiner and Krystal 1993). Newer ECT devices now provide quantitative estimates of various ictal EEG
indices, but their routine clinical utility is limited at present by
their sensitivity to EEG artifacts, variation in EEG lead placement, and interindividual and intraindividual variation in the
ictal electroencephalogram (Krystal et al. 1998).
Treatment Frequency and Number
A course of 6 to 12 treatments is usually required for treatment
of an acute episode of major or bipolar depression, although
fewer or more treatments are sometimes needed. Patients with
schizophrenia may require a larger number of treatments. In
the United States, the treatments are typically given thrice
weekly, but in Europe a twice-weekly schedule is often employed.
The treatments are continued until the patient has reached
a maximum level of response, at which point their frequency is
tapered in preparation for continuation treatment. As discussed above, the ECT treatment technique should be modified (e.g., switch stimulus electrode placement, increase stimulus dosage) if no improvement is seen by the sixth treatment.
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Electroconvulsive Therapy and Related Treatments
Alternative treatments should be considered if no response is
observed by 8 to 10 treatments, although in some cases a longer
series of treatments will be necessary.
Continuation/Maintenance Treatment
Because mood disorders are increasingly recognized as chronic,
relapsing conditions, successful acute treatment should be followed by some form of continuation or maintenance treatment
to prevent relapse or recurrence of the mood episode (see
Chapter 19, “Mood Disorders”). Studies in mixed-age samples
of adults with major depressive disorder have found 6-month
relapse rates as high as 50% for patients initially responsive to
antidepressants who were subsequently withdrawn from the
medications (Prien and Kupfer 1986). Relapse rates following
successful pharmacotherapy for major depression are substantially reduced by continuation of antidepressant medication at
full dosage (Frank et al. 1990). Similarly high rates of relapse
have been noted in adults with depression following ECT response when no form of continuation therapy was given (Jarvie
1954). The risk of relapse after successful acute ECT may be particularly high (especially in the first 4 months following ECT) in
patients with major depression who were resistant to medication or who displayed psychotic symptoms during their index
episode of illness (Grunhaus et al. 1995; Sackeim et al. 1993).
For continuation treatment in patients with major depression who are successfully treated with ECT acutely, there are
two options: combination pharmacotherapy or continuation
ECT. Controlled data suggest that continuation pharmacotherapy with nortriptyline and lithium (6-month relapse rate
of 39%) is superior to nortriptyline alone (6-month relapse
rate of 60%), which is in turn superior to placebo (6-month
relapse rate of 84%), in preventing relapse of major depression in adults who have responded to an acute course of ECT
(Sackeim et al. 2001). Continuation treatment with ECT is another option for continuation/maintenance treatment following successful acute ECT treatment, particularly in patients
who have psychotic depression or those who were resistant to
medication during the index episode (Fink 2007). Controlled
data in a mixed-age sample of adults with major depression
indicated that continuation ECT is comparable to continuation pharmacotherapy (nortriptyline and lithium) following
a successful acute course of brief-pulse bitemporal ECT given
at 1.5 times seizure threshold (6-month relapse rates of 37%
and 32%, respectively) (Kellner et al. 2006). These data extend
clinical reports of successful continuation ECT in elderly patients with major depression (Clark et al. 1989; Dubin et al.
1992; Loo et al. 1991; Monroe 1991; Thienhaus et al. 1990).
Continuation/maintenance ECT typically involves single
treatments administered on an outpatient basis, initially at
weekly intervals and then gradually reduced in frequency to
every 4–8 weeks, as the patient’s symptoms allow. The increased interval between treatments results in fewer cognitive
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side effects than during an acute course of ECT, and this has
led to the suggestion that bilateral electrode placement may be
preferred for continuation/maintenance ECT. The logistical
factors in outpatient ECT are defined in the report by the Task
Force on Ambulatory ECT of the Association for Convulsive
Therapy (Fink et al. 1996).
No controlled data have been reported to inform the
choice of whether to use pharmacotherapy or ECT for continuation treatment following successful ECT in patients with
major depression. In clinical practice many clinicians use the
rule “what got you well is what will keep you well,” which
would lead to a recommendation for ECT provided that it was
reasonably well tolerated. For at least some patients, however,
the logistical issues involved in months or years of continuation ECT are simply not manageable, and they prefer to take
their chances with medication.
As noted earlier in this chapter, patients with bipolar disorder may be successfully treated with ECT for acute mania or bipolar depression. Following such acute treatment, we generally
recommend at least 9–12 months of maintenance treatment
with ECT, although there are no controlled data on this issue.
During this maintenance ECT course, we continue to withhold
mood-stabilizing agents (e.g., lithium, anticonvulsants) to
avoid their potential complications (discussed in “Pretreatment Evaluation” earlier in this chapter). On the other hand,
some clinicians are concerned that breakthrough mood syndromes may occur as the frequency of the maintenance ECT
treatments is decreased, and thus they prefer to administer a
mood stabilizer between treatments, holding the dose a few
days before a scheduled ECT treatment to avoid potential complications. Most patients with bipolar disorder require lifetime
maintenance treatment with at least a mood stabilizer (e.g.,
lithium, anticonvulsants). Some clinical literature and our own
experience suggest that ECT may serve this role (alone or in
combination with psychotropic medication variously prescribed) in some patients who tolerate the procedure and related logistical issues well.
Following successful treatment with an acute course of
ECT, most patients with schizophrenia receive maintenance
treatment with antipsychotic medication (occasionally in
combination with other psychotropic medications). The potential role of maintenance ECT in such patients has not been
studied.
Adverse Effects of ECT and
Their Management
The safety of ECT compares favorably with that of any treatment
requiring general anesthesia. The mortality is variously reported
as approximating 1 death per 80,000 treatments (the same as for
general anesthesia for minor surgery) and may actually be de-
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creasing with improved management of underlying general
medical illnesses. To put these data into perspective, Abrams
(2002b) noted that ECT is 10 times safer than childbirth.
Kroessler and Fogel (1993) compared the mortality during
long-term follow-up of 65 depressed patients ages 80 and older
who had been treated with ECT or antidepressant medication.
Although the 2-year survival rate was 54% in the group treated
with ECT and 90% in the group treated with medication, this
group difference was probably related to more severe depression and physical illness in the patients who received ECT. The
course of ECT itself was remarkably well tolerated by these
elderly patients, with a median interval between ECT and
time of death of 20 months. The authors called for further attention to general medical comorbidity as a prognostic factor
in future outcome studies of geriatric depression. Abrams
(2002a) noted that the estimated mortality rate among community-dwelling elderly patients (∼0.26% per each 3 weeks)
was an order of magnitude higher than that observed after a
3-week course of eight ECT treatments in elderly patients
(∼0.016%). As noted earlier in “Medical Physiology of ECT,”
the major physiological impact of ECT is on the heart, vasculature, and brain.
Cardiovascular Side Effects
A proportion of elderly patients referred for ECT have serious
preexisting cardiovascular disease. Common cardiac conditions, such as hypertension, ischemic heart disease, atrial and
ventricular arrhythmia, aneurysm, and conduction system
disease, require evaluation and optimized treatment before
ECT to minimize any adverse effects from the hemodynamic
events that occur during ECT (Priebe 2000).
Uncontrolled retrospective studies comparing the cardiovascular complication rate of ECT in older and younger patients have found an increase in transient and treatable complications in elderly patients. In a nonblinded retrospective
chart review of 293 patients, Alexopoulos et al. (1984) found
cardiovascular complications in 9% of the patients ages 65
and older, compared with 1% of the patients under age 65.
Cardiac ischemia, arrhythmia, hypertension, and congestive
heart failure were the most common complications, although
the vast majority of complications were not clearly temporally
related to ECT and did not prevent the completion of treatment. Burke et al. (1987) conducted a similar retrospective
chart review of 136 subjects, 30% of whom were ages 60 and
older. Sine wave bilateral ECT was used in 85% of cases. These
investigators found a cardiorespiratory complication rate of
15% in patients ages 60 and older, compared with 3% in those
under age 60. Complications were correlated with the number
of cardiovascular medications the patient was receiving, with
more medication presumably indicating those patients with
more cardiovascular illness. These complications did not
affect treatment response. In a chart review of 81 elderly patients, Cattan et al. (1990) found a 36% cardiovascular complication rate with ECT in patients over age 80, compared
with 12% in younger geriatric patients. As would be expected,
the older patients had more general medical diagnoses and
were receiving more cardiovascular medication than were the
younger patients.
Two controlled studies of ECT in a total of 66 high-risk patients with cardiovascular disease have demonstrated the
safety of ECT in elderly individuals. Zielinsky et al. (1993)
compared the rate of cardiac complications in a group of 40
depressed patients (mean age 68.9 years; range 54–84 years)
with serious preexisting cardiac disease (left ventricular impairment, conduction delay, and ventricular arrhythmias)
with the rate of such complications in a group of 40 depressed
patients (mean age 68.3 years; range 55–83 years) without cardiac disease. Not surprisingly, the group with preexisting cardiac disease had more complications. Most of the complications were transient (e.g., brief arrhythmias or increases in
ectopy), however, and 38 of the 40 patients with cardiac disease were able to complete their course of ECT. Of note, this
group of depressed patients with cardiac disease had even
more difficulty with adverse cardiac effects from prior trials
of tricyclic antidepressants; 11 of the 21 patients previously
treated with tricyclic antidepressants had been forced to stop
tricyclic treatment because of cardiovascular complications.
Rice et al. (1994) used a case-control design to compare two
groups of patients over age 50 receiving ECT. One group consisted of 26 patients at increased risk for cardiac complications, and 27 patients at standard risk made up the other
group. Compared with the patients at standard risk for cardiac complications, patients in the high-risk group were older,
had received more medical consultations before ECT, and experienced more minor medical complications from ECT.
However, the two groups did not differ in terms of frequency
of major medical complications, and no patients died or experienced permanent cardiac morbidity from ECT.
The data just reviewed suggest that ECT is a low-risk procedure, even for elderly patients (Applegate 1997). It is rare for
ECT to be associated with severe cardiovascular complications, such as acute myocardial infarction, stroke, cardiovascular collapse, ventricular arrhythmia, or ruptured cerebral or
aortic aneurysm. Still, prospective studies, carefully controlled for pretreatment severity of cardiovascular and other
medical disease, are needed to evaluate the effects of age on
cardiovascular complications of ECT.
Increasingly sophisticated general medical management
during ECT helps to decrease the cardiovascular risk of treatment in elderly patients (Applegate 1997). The primary areas
of concern are bradycardia, tachycardia, hypertension, and
ventricular arrhythmia. Anticholinergic premedications (at-
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Electroconvulsive Therapy and Related Treatments
ropine and glycopyrrolate) may be used to prevent vagally induced bradycardia, but in elderly patients the use of these
medications may be more complicated by confusion, tachycardia, constipation, and urinary retention. The method of serial electrical stimulations to determine a patient’s seizure
threshold (described earlier) may involve administration of
subconvulsive stimuli, which may produce a vagal surge unaccompanied by the sympathetic outflow associated with a
seizure. The use of this method, as well as the presence of conduction delay on the ECG, suggests the need for premedication with an anticholinergic, particularly if the patient is also
receiving a beta-blocker medication. Outside of these clinical
scenarios, some practitioners reserve the use of anticholinergic premedication for patients who develop substantial
bradyarrhythmias during ECT.
A related issue is the safety of ECT in a patient with a vagus
nerve stimulator (see Chapter 11, “Brain Stimulation Therapies”), the effects of which might be thought to be problematic if they add to the vagal effects of ECT. Although experience is limited, the safe use of ECT in a patient with the vagus
nerve stimulator has been reported (Husain et al. 2002).
Although hypertension and tachycardia (mediated by sympathetic activation) are common during ECT, they are well
tolerated by most patients, including elderly individuals
(Webb et al. 1990). Therefore, it is usually unnecessary to routinely blunt the cardiovascular response to ECT in elderly patients unless such changes are extreme or are clearly associated
with evidence of cardiovascular compromise. These robust
hemodynamic responses may be attenuated by short-acting
intravenous beta-blockers, such as labetalol or esmolol, or by
nitroglycerine preparations (Howie et al. 1990; Stoudemire et
al. 1990). It should be kept in mind that beta-blockers have
anticonvulsant effects, and their use during ECT may limit the
intensity of the ECT seizure and, in turn, its therapeutic potency. In addition, the acute use of antihypertensive medication may lead to clinically significant hypotension in elderly
patients during the recovery period. Finally, in patients receiving adrenergic blockers, anticholinergic premedication
should be considered so as to prevent a disproportionate decrease of sympathetic tone below parasympathetic tone, with
resultant bradycardia (Abrams 2002b).
Marked posttreatment ventricular ectopy (multifocal or
several consecutive premature ventricular contractions) may
be treated with lidocaine (1–1.5 m/kg body weight). Because
of its anticonvulsant properties, lidocaine should be given after termination of the seizure (Drop and Welch 1989). Stoudemire et al. (1990) found that ventricular ectopy could also
be reduced by pretreatment with labetalol. The presence of a
properly functioning implanted cardiac pacemaker is not a
concern with ECT, provided the usual electrical safety precautions are followed (Abrams 2002b).
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Cerebral Side Effects
There is no evidence that ECT causes structural brain damage
(Devanand et al. 1994; Weiner 1984). Carefully controlled prospective brain imaging studies in humans reveal no changes in
brain structure for up to 6 months after a course of ECT (Coffey 1993; Coffey et al. 1991), and other studies using proton
magnetic resonance spectroscopy find that ECT is not associated with a decrease in the N-acetylaspartate signal, a sign of
cell atrophy (Ende et al. 2000; Pfleiderer et al. 2003). Neuropathological studies in elderly humans who received numerous lifetime ECT treatments reveal no evidence of ECT-related
injury (Scalia et al. 2007). Neuropathological studies in animals, including cell counts in regions thought to be at risk, reveal no evidence of brain damage when the seizures are induced under conditions that approximate standard clinical
practice (i.e., when the seizures are temporally spaced, relatively brief, and modified by oxygenation and muscle relaxation). Furthermore, studies of the pathophysiology of seizure-induced structural brain damage in animals indicate that
the conditions necessary for injury do not apply to the modern
practice of ECT (Weiner 1984). In this regard, a brain metabolic imaging study of elderly patients with depression found
no evidence of brain perfusion abnormalities at 1 year following a successful course of ECT (Navarro et al. 2004).
The robust cardiovascular responses associated with the
ECT seizure have raised a theoretical concern that they may
precipitate cerebrovascular events. The incidence of cerebrovascular complications with ECT is exceedingly rare, however.
We are aware of only one reported case of ischemic stroke after
ECT that was confirmed by brain imaging (Bruce et al. 2006).
ECT has been given successfully to patients with cerebral aneurysms, with close management of blood pressure elevation
(Krystal and Coffey 1997). An intracerebral hemorrhage reported in a normotensive patient during ECT was probably
related to cerebral amyloid angiopathy (Weisberg et al. 1991).
We know of no other reported case of intracerebral hemorrhage with ECT.
Cognitive Side Effects
The cognitive side effects of ECT include acute postictal confusion, impaired retrograde and anterograde memory, and
occasionally interictal delirium. The extent of these adverse
effects is related to certain patient factors, such as increased
age (see Gardner and O’Connor 2008 for a review), general
medical disease burden, and preexisting cognitive impairment, and to ECT technique factors (sine wave stimulus waveform, bitemporal electrode placement, grossly suprathreshold
stimulus dosage, increased number or frequency of treatments, poor oxygenation during the procedure, and certain
concomitant medications, such as lithium and anticholin-
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ergics) (see The Journal of ECT, Volume 24, No. 1, Special Issue: Cognitive Effects of ECT, 2008).
Acute Postictal Disorientation
Most patients experience mild disorientation immediately
upon awakening during the post-ECT recovery process, which
typically resolves within an hour or so (Calev et al. 1993). In a
study focusing on elderly patients, Fraser and Glass (1978)
measured time to recovery of full orientation in nine elderly
patients with depression who received ECT in which electrode
placement alternated (e.g., unilateral placement in one treatment followed by bilateral placement in the next treatment).
When comparing these reorientation times with those reported
in the literature for younger patients, the investigators observed
that recovery in elderly patients took five times longer for unilateral treatment and nine times longer for bilateral treatment.
Recovery time after bilateral ECT increased cumulatively over
the course of ECT and with closer spacing of treatments. No
such relationship was found for unilateral ECT. In a subsequent
study of 29 elderly patients with depression randomly assigned
to courses of either unilateral (n=13) or bilateral (n=16) sine
wave ECT, Fraser and Glass (1980) found significantly longer
reorientation times after the fifth ECT session among patients
receiving bilateral treatments (32.8 minutes) than among those
receiving unilateral treatments (9.5 minutes). In contrast to the
group undergoing bilateral ECT, patients receiving unilateral
ECT had a significant reduction in recovery time from the first
to the last treatment.
In a study of subjective side effects during ECT, Devanand
et al. (1995) found that older patients actually reported fewer
severe cognitive symptoms (i.e., confusion/disorientation and
amnesia) than did younger patients.
Agitated Delirium on Emergence From Anesthesia
Approximately 10% of patients receiving ECT experience an
acute agitated delirium on emergence from anesthesia, characterized by restlessness, disorientation, combativeness, and
poor response to commands. Age does not appear to be a risk
for this complication (Devanand et al. 1989). This complication is usually managed effectively with supportive care, although occasionally treatment with intravenous benzodiazepines (e.g., midazolam, diazepam) or other sedatives (e.g.,
methohexital, propofol) may be required.
Interictal Delirium
In a small proportion of patients, ECT is associated with more
prolonged disorientation and even frank interictal delirium.
Most studies evaluating interictal delirium in elderly patients
have used disorientation as a measure rather than the full
DSM criteria for delirium. In a retrospective study involving
136 patients receiving mainly bilateral sine wave ECT, Burke et
al. (1987) found disorientation (confusion severe enough to
alter the treatment plan) in 18% of patients older than age 60,
compared with 13% of younger patients. This incidence increased to 25% for patients over age 75. In a retrospective study
in which mostly bilateral (waveform not specified) ECT was
administered, Alexopoulos et al. (1984) found a somewhat
greater incidence of confusion (disorientation to time, place,
and person) in elderly patients (12.6%) than in younger patients (9.6%). Cattan et al. (1990) conducted a study involving
primarily bilateral or combination bilateral-unilateral sine
wave ECT and found a nonsignificant trend for more frequent
severe disorientation (defined functionally by interference in
ward activities) in elderly patients over age 80 (59%, n=39),
compared with those patients 65–80 years old (45%, n=42).
In the study by Alexopoulos et al. (1984), elderly patients
with a history of underlying brain disease were found to have
higher levels of severe post-ECT confusion than were the
young patients, suggesting that baseline cerebral impairment
may increase the risk of adverse cognitive effects of ECT.
In several studies, subcortical brain disease has been implicated in the development of interictal delirium with ECT. We
have found subcortical gray and white matter lesions to be
more extensive in elderly patients who developed a prolonged
interictal delirium during a course of ECT (Figiel et al. 1990).
Still, the majority of these patients were able to continue ECT,
with no decline in expected treatment response. All patients
were free of delirium 1 week after ECT (Coffey et al. 1989;
Figiel et al. 1990). The specificity of subcortical disease in producing delirium after ECT was further suggested by Martin et
al. (1992), who found that patients with ischemic lesions of the
caudate nucleus had a 92% incidence of delirium during ECT.
Patients with a previous stroke in other brain regions had the
same incidence of delirium as did a group of elderly depressed
nonstroke control subjects receiving ECT (Martin et al. 1992).
In a prospective study of seven consecutive patients with Parkinson’s disease, Figiel et al. (1991) found a 100% incidence of
interictal delirium during a course of ECT. The delirium lasted
7–21 days, longer than is typical, but 86% of patients recovered
from depression.
In summary, although the duration and severity of acute
post-ECT disorientation may increase with age, the majority
of elderly patients appear to recover their orientation within
60 minutes of the treatment. In the small percentage of elderly
patients who develop more prolonged confusion or frank delirium, underlying cerebral impairment may be contributory,
especially dysfunction of the basal ganglia. Clearly, more research is needed in a larger number of elderly patients to characterize post-ECT confusion and to identify its risk factors, including the effects of preexisting cerebral impairment.
Reprinted from Coffey CE, Cummings JL (eds): The American Psychiatric Publishing Textbook of Geriatric Neuropsychiatry, Third Edition. Copyright © 2011 American Psychiatric Association.
Electroconvulsive Therapy and Related Treatments
Amnesia
The depressive syndrome (as well as many other psychiatric syndromes) causes impairment in new learning. An acute course of
contemporary brief-pulse ECT may improve this deficit as it
improves the depression, but the treatment also causes a new
deficit in memory such that newly learned information is rapidly forgotten. Explicit (especially autobiographical) memories
are affected (implicit memory is spared), and both anterograde
and retrograde deficits are seen, particularly for events that occurred closest to the time of treatment. This memory deficit is
typically relatively mild and is presumed to be secondary to
transient disruption of medial temporal lobe function. The anterograde amnesia typically resolves within a few weeks of ECT,
whereas the retrograde deficit may resolve more gradually. Persistent and severe retrograde amnesia has been reported rarely
following ECT (Sackeim 2000), but the interpretation and significance of such reports remain controversial (Abrams 2002a).
Given the large body of data on the amnestic effects of ECT,
it is surprising that there has been relatively little controlled research on age as a risk factor (Abrams 1997; Calev et al. 1993;
Fink 1979). Some (Fromholt et al. 1973; Heshe et al. 1978) but
not all (d’Elia and Raotma 1977; Strömgren et al. 1976) early
studies found that ECT-induced amnesia is worse in older patients. Zervas et al. (1993) examined age effects on memory in a
study comparing twice-weekly and three-times-weekly briefpulse bilateral ECT administered using contemporary techniques (given at “moderately suprathreshold” stimulus intensity). The sample consisted of 42 inpatients with a mean age
(±SD) of 53.5±16.1 years; no patient was older than 65 years,
however. Correlations were found between age and decrements
in retrograde memory 1–3 days after the end of ECT but not at
1 month or 6 months posttreatment. Age was also correlated
with decrements in verbal anterograde memory acutely and
1 month after ECT (but not 6 months after ECT) and with
changes in figural anterograde memory acutely and 6 months
after ECT. McElhiney et al. (1995) examined autobiographical
memory in a mixed-age sample (mean age [±SD] 54 ±13.9
years) of 75 patients with depression randomly assigned with
regard to electrode placement and stimulus intensity. Age was
found to be a predictor of lower recall of autobiographical
memories after ECT. In a follow-up report on this sample, the
pre-ECT modified Mini-Mental State Examination score was
predictive of the extent of retrograde autobiographical amnesia both 1 week and 2 months after ECT (Sobin et al. 1995).
This study provided evidence in support of the conventional
clinical wisdom that preexisting cognitive deficit is a risk factor
for more severe ECT-induced amnesia.
Memory performance has been reported to improve with
successful ECT in elderly patients with the pseudodementia of
depression (Reynolds et al. 1987; Stoudemire et al. 1995). In the
study by Fraser and Glass (1980) described earlier, all elderly pa-
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tients showed impairment of memory function before ECT; during treatment, however, memory improved and was normal in all
patients by 3 weeks after completion of the ECT course. No group
differences were found on the basis of electrode placement.
Relatively little research has been done regarding the effects of age on subjective memory complaints after ECT (Prudic et al. 2000). As noted previously, Devanand et al. (1995)
found that older patients actually reported fewer severe cognitive symptoms (i.e., confusion/disorientation and amnesia)
than did younger patients.
In summary, controlled data appear to support the clinical
wisdom that elderly patients are at greater risk for the cognitive side effects of ECT. More work is needed in a larger number of elderly patients (especially very old patients) to characterize the extent and severity of ECT-induced amnesia and to
identify relevant risk factors, including the effects of preexisting cerebral impairment.
Managing Cognitive Side Effects During ECT
Recommendations for lessening ECT amnesia in elderly patients focus on risk factors related to the patients, as well as on
aspects of the treatment technique. Patients should have their
general medical health optimized as much as possible before
commencing ECT, and concomitant medications with potential adverse effects on memory should be discontinued when
possible. The ECT technique should employ proper anesthetic
technique, a contemporary constant-current brief-pulse device, and careful consideration of the relative merits of unilateral versus bilateral stimulus electrode placement. If intolerable cognitive side effects develop, the frequency of treatments
could be reduced from thrice to twice weekly (e.g., Monday
and Friday). A variety of “memory-enhancing” pharmacological agents (e.g., indomethacin, piracetam, naloxone, choline,
donepezil, and herbals) have been explored in animal models
of ECT as well as in humans, but the data are insufficient to
support routine clinical use at this time (Prakash et al. 2006;
Prudic et al. 1998; Rao et al. 2002; Tang et al. 2002).
Side Effects in Other Organ Systems
Other organ systems that may be impaired in elderly patients
need to be evaluated before ECT and include the lungs, bones,
eyes, and teeth. Pulmonary status should be optimized before
ECT. Patients with severe chronic obstructive pulmonary disease and carbon dioxide retention may require special ventilatory strategies during the treatment (Abrams 2002b). Pneumonia secondary to aspiration of gastric contents may occur
rarely during ECT (Alexopoulos et al. 1984; Karlinsky and
Shulman 1984).
Patients with osteoporosis, spinal disk disease, or spondylosis may require increased muscular relaxation during ECT.
Such patients may require succinylcholine doses of at least 1–
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1.5 mg/kg body weight, and they require careful attention to
clinical evidence of adequate relaxation (e.g., loss of reflexes or
tone, and disappearance of fasciculations) before delivery of
the stimulus. Kellner et al. (1991b) reported the safe treatment
of a patient with osteoporosis and cervical spondylosis with
multiple subluxations of the cervical spine using succinylcholine doses of 1.3 mg/kg weight.
Because ECT produces a transient increase in intraocular
pressure, patients with chronic open-angle glaucoma should
receive their eyedrops before ECT. As noted earlier in “Technique of ECT,” treatment with echothiophate, an irreversible
cholinesterase inhibitor, should be stopped several days before
ECT. Patients with acute closed-angle glaucoma or retinal detachment should be stabilized before ECT and watched closely
by an ophthalmologist during an ECT course.
When a patient’s teeth are loose, decayed, or asymmetrical,
the risk of dental injury during ECT may be increased. A major
portion of malpractice litigation with ECT is related to dental
issues (Slawson 1985). A specially designed bite block must be
inserted before delivery of the ECT stimulus. The tongue,
cheeks, and lips must be kept clear of the clenching teeth. The
bite block should be used even in edentulous patients. Occasionally, upper or lower dentures may be kept in place during
the treatment to facilitate airway management. In patients with
only a few remaining, and possibly loose, teeth, dental consultation or alternative bite block strategies (with the aim of shifting bite pressure to the molars) may be helpful (Welch 1993).
ECT in Elderly Patients With
Neurological Disorders
Although mood disturbances are common in patients with
neurological disorders, there are relatively few controlled data to
inform their treatment (see chapters in Part IV, “Neuropsychiatric Syndromes and Disorders”). There are no controlled data
on the safety and efficacy of ECT in depressed elderly patients
with concomitant neurological disorders (Coffey et al. 2007;
Van der Wurff et al. 2003); however, a substantial clinical experience suggests that ECT may be an important therapeutic option for many of these patients (Coffey et al. 2007; Evans et al.
2005; Krystal and Coffey 1997), particularly when there is an urgent need for rapid clinical improvement or when pharmacotherapy has been either ineffective or poorly tolerated. The
safety of ECT in these patients depends critically on optimizing
the treatment of the underlying neurological (and all other general medical) conditions and on modifying the technique of
ECT where indicated to mitigate the procedure’s physiological
effects (e.g., increased intracranial pressure, increased blood
pressure) (Coffey et al. 2007). In all such cases, a careful risk-
benefit analysis should be conducted during the pre-ECT evaluation. In the following sections, we discuss some of the more
common conditions in which ECT may be considered as a treatment option for elderly patients with a neurological disorder.
Dementia
As discussed in Chapter 16, “Alzheimer’s Disease and the
Frontotemporal Dementia Syndromes,” depression is common in patients with dementia, and it has a critical impact on
patients’ survival and functional recovery. Treatment with antidepressant medications may help some but not all of these
patients (see Chapter 19, “Mood Disorders”).
A small clinical literature suggests that ECT may also
be safe and effective for treating depression in patients with
degenerative dementia, including those with Alzheimer’s disease, vascular dementia, Friedreich’s ataxia, and probable Lewy
body dementia. In a literature review of 56 patients with dementia who received ECT for depression, Price and McAllister
(1989) found the rate of response of depression to be 73%.
ECT effectively treated depression in several subtypes of dementia, including senile dementia of the Alzheimer’s type,
multi-infarct dementia, and normal-pressure hydrocephalus,
as well as the dementias of Parkinson’s disease and Huntington’s disease. Location of the stimulus electrodes was not specified in the majority of the cases reviewed. Nearly one-third of
patients with dementia also had an improvement in cognition
after ECT. Delirium was a relatively infrequent complication of
ECT in these patients (overall occurrence of 21%), clearing by
the time of discharge in all but 1 patient. Nelson and Rosenberg (1991) found that the ECT outcomes were similar in their
21 elderly patients with dementia and major depression, compared with a reference group of 84 elderly depressed patients
without dementia. Rao and Lyketsos (2000) described their experience with 31 consecutive patients with dementia treated
with ECT over a 5-year period at their institution. Approximately 68% of the sample was “clearly improved,” and the
most common adverse event was a transient delirium (seen in
49%). Rasmussen et al. (2003) described 7 patients with presumed Lewy body dementia who responded to ECT and tolerated the treatment well. Although these data are reassuring,
prospective studies are needed to determine the efficacy and
side effects of ECT in depressed patients with dementia.
To minimize cognitive side effects of ECT in patients with
dementia, the ECT practitioner needs to pay special attention
to issues of concomitant medications (including cholinesterase inhibitors, which may prolong the effect of succinylcholine as well as lower seizure threshold), electrode placement,
and frequency of treatments (discussed earlier in “Technique
of ECT”). Particular attention must be paid to issues of informed consent (see Chapter 14, “Ethical and Legal Issues”).
Reprinted from Coffey CE, Cummings JL (eds): The American Psychiatric Publishing Textbook of Geriatric Neuropsychiatry, Third Edition. Copyright © 2011 American Psychiatric Association.
Electroconvulsive Therapy and Related Treatments
Cerebrovascular Disease and
Cerebral Aneurysm
As discussed in Chapter 25, “Cerebrovascular Disease,” depression is common following stroke, and it has a critical impact on the patient’s survival and functional recovery. Treatment with antidepressant medications may help some but not
all such patients (see Chapter 19, “Mood Disorders”).
Case reports and case series suggest that ECT may also be
safe and effective for treating poststroke depression. In a retrospective chart review of 14 patients with poststroke depression
(mean age 66 years) treated with ECT at Massachusetts General
Hospital, Murray et al. (1986) found that 86% had marked improvement in depression after ECT. Apparently, no patient exhibited any worsening of neurological deficit, and although formal measures of cognitive status were not reported, 5 of the 6
patients with “cognitive impairment” before ECT showed lessening of this deficit after ECT. Currier et al. (1992) published
retrospective data on 20 geriatric patients with poststroke depression treated with ECT at the same hospital, with predominantly nondominant unilateral electrode placement being
used. A “marked or moderate response” to ECT was observed
in 95% of the patients. No patient experienced any exacerbation
of preexisting neurological deficits, but 3 patients exhibited
“minor encephalopathic complications” (prolonged postictal
confusion and amnesia) and 2 patients developed “severe interictal delirium requiring neuroleptics.” Of note, 7 of their patients (37%) relapsed within a mean of 4 months after stopping
ECT, despite ongoing maintenance drug therapy.
Elderly patients with no clinical history of stroke often have
subcortical white matter hyperintensities on magnetic resonance images, which are believed to be evidence of ischemic
cerebrovascular disease (see Chapter 19). Coffey et al. (1989)
found a high rate (82%) of response to ECT in depressed patients with these magnetic resonance imaging findings, many of
whom had been refractory to antidepressant drug therapy. In
addition, the majority of the patients tolerated the course of
ECT without major systemic or cognitive side effects. This positive outcome with ECT is especially notable given other data
suggesting that subcortical ischemic disease may be associated
with depressive illness that is resistant to treatment with antidepressant medications (Baldwin et al. 2004; Iosifescu et al. 2006).
The safety of ECT in a patient with cerebrovascular disease
requires a thorough diagnostic assessment and optimal preECT treatment of the cerebrovascular disease and any other
general medical conditions. A diagnostic evaluation must clarify the precise etiology of the cerebrovascular event (arterial ischemic stroke vs. cerebral venous sinus occlusion vs. hemorrhagic stroke), and the treatment for that condition must be
optimized. The clinician must also assess the potential effect of
the underlying vascular disease on other organs impacted by
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ECT, notably the heart, and institute treatment when indicated.
Before commencing ECT, it is preferable to wait at least several
weeks if possible after the cerebral infarct to allow time for fragile cerebral vessels and tissue to heal, thereby reducing the theoretical risk of rupture from the increased cerebral blood flow.
Occasionally, the ECT practitioner may employ antihypertensive medications during the ECT procedure to lessen the hemodynamic effects of the electrical stimulus and seizure.
The authors of several case and small series studies have reported on the safe and effective use of ECT in patients with intracranial aneurysm (including coil embolization) or various
malformations, including arteriovenous malformations, venous angiomas, and cavernous hemangiomas (Okamura et al.
2006; Rasmussen and Flemming 2006; Zahedi et al. 2006). We
are not aware of a report of patients with untreated cerebral
aneurysm or malformation who experienced an intracranial
hemorrhage with ECT. Nevertheless, we advise surgical correction of such lesions when indicated, before commencing ECT. If
such surgery is not indicated, pharmacological attenuation of
the hemodynamic responses during ECT should be considered.
Parkinson’s Disease
As discussed in Chapter 24, “Parkinson’s Disease and Movement Disorders,” depression is common in patients with Parkinson’s disease, and it has a critical impact on patients’ survival and functional recovery. Treatment with antidepressant
medications may help some but not all such patients (see
Chapter 19, “Mood Disorders”).
A small clinical literature suggests that ECT may be safe
and effective for both the mood disorder and the motor disturbance associated with Parkinson’s disease (reviewed by
Kellner and Bernstein 1993). Interestingly, some patients experience improvement in motor symptoms but not improvement in mood, or vice versa (Kellner and Bernstein 1993).
A group of Swedish investigators (Andersen et al. 1987) performed the most methodologically rigorous trial of ECT in
Parkinson’s disease. In this double-blind, controlled, crossover
design comparison of real ECT and sham ECT, 9 (82%) of 11
nondepressed elderly patients with the on-off phenomenon experienced substantial improvement in parkinsonian symptoms
with ECT, with the improvement lasting 2–6 weeks. Sham ECT
was ineffective. Nine patients received bilateral ECT (eight responded, one did not), and two patients received right unilateral ECT (one responded, one did not). Five to six treatments
were given during the active phase of the trial. The stimulusdosing strategy was not fully detailed in the report.
In a prospective naturalistic study, Douyon et al. (1989)
studied seven patients with both Parkinson’s disease and major depression. Substantial improvement in motor function
was noted after only two bilateral treatments. Following an av-
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erage of seven bilateral ECT treatments, with “just above
threshold” stimulus dosing, mean New York University Parkinson’s Disease Rating Scale scores decreased from 65 to 32
(51% improvement). Patients remained well, without further
ECT, for 4 weeks to 6 months. Although initial scores on the
Hamilton Rating Scale for Depression were determined for all
seven patients (all scores were greater than 20), follow-up
scores were determined for only four patients (these scores decreased by a mean of 50%). In another prospective naturalistic
study, Zervas and Fink (1991) described the ECT treatment of
four nondepressed elderly patients with severe, refractory Parkinson’s disease. Three of the four patients received bilateral
ECT. Stimulus-dosing strategies were not specified. Improvement in parkinsonism rating scores of 20%–40% was observed. Two patients were successfully treated with ongoing
maintenance ECT, but once it was discontinued, the parkinsonism returned in both patients within 4–6 weeks. Aarsland
et al. (1997) reported on two additional patients whose Parkinson’s disease was successfully treated with maintenance ECT,
and others have reported its utility for this purpose as well
(Krystal and Coffey 1997; Wengel et al. 1998). Finally, ECT has
also been found to be effective for neuroleptic-induced parkinsonism (Hermesh et al. 1992).
Because patients with parkinsonism may be at an increased
risk of interictal delirium with ECT, we recommend commencing treatment with unilateral nondominant electrode
placement. ECT may also be associated with dopaminergic
side effects (dyskinesia, psychosis), in which case the dose of
levodopa or other antiparkinsonian agents may need to be reduced carefully during the course of treatments. We do not recommend altering the dose of levodopa prior to ECT, because
doing so may precipitate severe bradykinesia. Finally, ECT may
also be performed safely in patients with Parkinson’s disease
and a deep brain stimulator, because the brain electrodes do
not become dislodged or heated (Bailine et al. 2008).
Brain Tumor or Mass
Intracranial mass lesions and increased intracranial pressure
are among the most serious risk factors for ECT. Patients with
these conditions are at risk for developing noncardiogenic
pulmonary edema, cerebral edema, brain hemorrhage, and
cerebral herniation (Krystal and Coffey 1997; Maltbie et al.
1980). ECT may be administered safely and effectively to
patients with small or slow-growing intracranial tumors or
arachnoid cysts that have no associated swelling or increased
intracranial pressure (Abrams 2002b; Coffey et al. 1987). The
risks to individuals with more substantial masses may be reduced by surgically removing or debulking the mass when
possible, and by trying to diminish the surrounding edema
(e.g., steroids, diuretics, or hyperventilation during the treat-
ment) and the rise in intracranial pressure during the treatment (e.g., by pretreatment administration of antihypertensive agents) (Rasmussen et al. 2007b). There is no report of
safely delivered ECT prospectively given to a patient with documented increased intracranial pressure (Abrams 2002b).
Subdural hematomas may require evacuation before ECT
(Abrams 2002b).
Patients with normal-pressure hydrocephalus, including
those with a shunt, may be treated safely and effectively with
ECT, provided the shunt is determined to be patent, although
such patients may be at increased risk of cognitive side effects.
These patients (as well as others with prior brain surgery or
head injury) may have a skull defect, which may increase the
risk of cognitive side effects or injury if the stimulus electrode is
placed nearby (allowing greater current density to be administered to the brain). In such cases, repositioning of the stimulus
electrode is indicated.
Psychosocial Issues
In addition to its myriad biological effects, ECT has important
intrapsychic and interpersonal effects. A powerful treatment,
during which the patient is put to sleep and has an electrical
stimulus delivered to the head, may arouse predictable fears
and fantasies in the patient. Issues of trust and autonomy over
one’s body while in a vulnerable position may predominate,
especially in patients with a history of trauma. Patient education—in particular, educational videotapes—may reduce
these fears. Patients who are vulnerable to idealized fantasies
of a nurturing, all-caring, supportive other may overvalue the
ECT procedure and practitioner. Conversely, these patients
may excessively devalue the treatment when their distorted
expectations are not realized. Such patients may be at increased risk for a bad psychological outcome from the treatment. The ECT practitioner should challenge overidealization
of the treatment, and the informed consent process should be
firmly grounded in factual information. We have also found
that for some patients, the experience of ECT is markedly improved if a family member or significant other is present during the procedure.
Patient attitude surveys have found that although ECT is
poorly understood, those undergoing ECT typically find the
experience no more upsetting than a trip to the dentist (Fox
1993; Hughes et al. 1981; Malcolm 1989). These results are
limited, however, by a variety of methodological issues (Rose et
al. 2003). Only a few studies have systematically examined the
effects of age on patients’ perception and knowledge of ECT.
Malcolm (1989) found that patients over age 65 had less
knowledge of the procedure before treatment and were also
less fearful of it. In addition, fewer elderly patients viewed the
treatment as frightening after completing a course of ECT. Sie-
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Electroconvulsive Therapy and Related Treatments
naert et al. (2005) found no relation between a patient’s age
and degree of satisfaction with ECT, which in general was quite
high even in the presence of memory complaints.
Medicolegal issues surrounding the use of ECT with elderly patients include the informed consent process (discussed earlier in this chapter), do-not-resuscitate (DNR) orders, and consideration of driving after ECT (see Chapter 14,
“Ethical and Legal Issues”). A patient with DNR status may
still experience improved quality of life with aggressive treatment of his or her affective disorder and may still be considered for ECT (Sullivan et al. 1992). In such cases, strategies for
the management of major complications that could occur
during ECT should be discussed with the patient and the family before treatment. Patients should not drive after an ECT
course until cognitive side effects have substantially resolved
(Fink 1994). This issue may be an especially sensitive one for
elderly patients who consider driving a means of maintaining
their mobility and functional independence.
Financial concerns are of increasing importance in today’s
cost-conscious health care marketplace. A growing literature
suggests that ECT has economic advantages over other forms
of treatment for severe mood disorders. The cost-effectiveness
of ECT has been demonstrated both for inpatient treatment of
the index episode and for maintenance therapy on an ambulatory basis (Markowitz et al. 1987; McDonald et al. 1998; Olfson et al. 1998; Steffens et al. 1995). Despite these advantages,
there remains much variation in ECT reimbursement patterns, and it is not uncommon to encounter payers who will
reimburse only for ECT when given on an inpatient basis. In
addition, reimbursement rates are very low and thus discourage the use of this safe and highly effective treatment.
Novel Techniques for Inducing
Therapeutic Seizures
As discussed earlier in the section “Cognitive Side Effects,”
data suggest that the efficacy and cognitive side effects of ECT
may be determined in part by the site of the seizure initiation
and by the pattern of seizure generalization. The antidepressant effects of ECT may be correlated with functional changes
in prefrontal (among other) brain regions, whereas the amnestic effects of ECT are associated with functional and synaptic changes in the medial temporal lobes. Thus, at least in
theory, the goal of the “brain stimulation” specialist is to employ strategies that induce relatively focal seizures in regions
that modulate mood (e.g., perhaps the prefrontal region) and
that limit spread of the seizure to the medial temporal region.
The use of unilateral nondominant stimulus electrode
placement is one such strategy to spatially target the stimulus.
Although it produces differences in seizure initiation and
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spread, as well as substantial differences in cognitive side effects relative to bilateral stimulation, the resultant seizure is
still bilaterally generalized. A recent strategy to spatially target
even more precisely the electrical stimulus in ECT is known as
focal electrically administered seizure therapy (FEAST). This
experimental technique couples novel electrode geometry
with unidirectional (anode-cathode) stimulation. In nonhuman primates, FEAST has been shown to be a safe and reliable
means of inducing a variety of seizure types, from focal to generalized (Berman et al. 2005). Research is under way to determine the applicability of FEAST in humans.
Substantial challenges remain, however, in the use of electrical stimulation to induce focal brain seizures, as a result of
the physics of brain stimulation. When electricity is applied
directly to the scalp, its flow is impeded by the scalp and the
skull, resulting in a “smearing” of the electrical stimulus and a
relative broadening of the field of brain stimulation. These
factors are likely confounded by individual differences in the
anatomy of the scalp and skull, making standardization across
patients difficult. Therefore, research has turned to the use of
other stimuli to induce a relatively focal therapeutic brain seizure, and among the most promising is magnetic stimulation.
As discussed in Chapter 11, “Brain Stimulation Therapies,”
seizures may be a side effect of repetitive transcranial magnetic
stimulation when administered at high stimulus intensity. This
observation has led to the suggestion that repetitive transcranial magnetic stimulation might be used as a means of inducing therapeutic seizures, a technique termed magnetic seizure
therapy (MST). Relative to ECT, MST would have a theoretical
advantage of more precise targeting of the stimulus, because
magnetic fields pass through tissue (including scalp and skull)
without impedance (i.e., without smearing). In addition, MST
typically delivers magnetic stimulation that is relatively superficial, penetrating only ∼2–4 cm beneath the scalp. Thus, MST
offers the theoretical advantage of relatively more precise targeting of the seizure to superficial cortical structures presumed
to mediate mood (perhaps the prefrontal brain region) while
at the same time sparing stimulation of deeper structures, such
as the hippocampus, associated with amnestic side effects
(Lisanby and Peterchev 2007).
Indeed, research in nonhuman primates has demonstrated
that 1) relative to electrical stimulation, the current induced by
MST is less intense and relatively more discrete; and 2) the resulting seizures are relatively more focal and are associated
with less neuroendocrine, autonomic, and neuroplastic responses, as well as with more benign acute cognitive side effects
(Spellman et al. 2008). Several dozen patients with depression
have now received MST on an experimental basis, and in general they have tolerated the procedure without any major adverse or unanticipated effects (for a review, see Marcolin and
Padberg 2007). Consistent with the studies in nonhuman pri-
Reprinted from Coffey CE, Cummings JL (eds): The American Psychiatric Publishing Textbook of Geriatric Neuropsychiatry, Third Edition. Copyright © 2011 American Psychiatric Association.
296
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mates, these patients had more focal and less physiologically
“intense” seizures than with ECT, and patients experienced less
disorientation and fewer short-term amnestic side effects, at
least for some types of memory (i.e., those mediated by the
temporal lobes). No differences were seen between ECT and
MST seizures in those cognitive functions presumably mediated by prefrontal brain regions. Thus, MST appears feasible
and safe, and the fact that it has relatively mild autonomic effects might be a decided advantage over ECT in elderly patients
with cardiovascular risks. More research is needed, however, to
determine the efficacy of MST and to clarify a host of technical
issues (coil selection, parameters of stimulation, pulse characteristics, power requirements, optimal anesthesia, and so
forth) that impact the neurobiological effects of this intriguing
procedure.
Conclusion
More than 70 years after its introduction, ECT remains a cornerstone of the treatment of severe affective disorder and selected
other neuropsychiatric illnesses in elderly patients. ECT also appears to be an effective treatment in patients with preexisting
brain disease and in some cases may even have a beneficial effect
on the underlying neurological disorder. Continued advances in
ECT technique have improved the efficacy of the procedure and
reduced the risk of severe side effects. However, few controlled
studies have compared the efficacy and safety of ECT versus
pharmacotherapy in elderly patients. Further study is needed to
determine the impact of age-related changes in brain structure
or function and of preexisting cerebral disease on the beneficial
effects of ECT in elderly patients. The mechanism of action of
this important treatment remains to be fully elucidated.
Key Points
• ECT is an important treatment option for elderly patients with certain neuropsychiatric illnesses. It is most commonly used for the treatment of severe
medication-resistant depression. For urgently ill depressed patients, ECT may
be used as first-line treatment. It is also used to treat mania, schizophrenia,
and catatonia. It is effective in depression-complicating dementia, stroke, and
Parkinson’s disease. It has also been shown to have a beneficial effect on the
motor symptoms of Parkinson’s disease.
• The cardiovascular and cerebral physiological changes that occur during ECT
are particularly relevant for elderly patients with complex medical illnesses.
Modern anesthesia techniques (e.g., using ultra-brief-acting barbiturates,
muscle relaxants, and intravenous beta-blockers to control cardiac rate and
blood pressure) make the procedure remarkably safe. The cognitive effects of
ECT, particularly recent memory loss, may be mitigated by careful attention to
technical issues in the administration of the procedure, including the use of
right unilateral electrode placement and optimal stimulus dosing.
• ECT is most commonly administered as a series of 6 to 12 treatments targeting
acute depressive or psychotic symptoms. It can also be used as a continuation
or maintenance treatment, given on an outpatient basis every 1–8 weeks, with
the goal of preventing a subsequent episode of illness.
• Novel and still experimental brain stimulation techniques hold out the possibility of inducing more focal cerebral seizures or stimulation but are not yet
available for widespread clinical use. Careful attention to patient and family
education and the informed consent process are important aspects of making
ECT acceptable and nonthreatening to patients.
Reprinted from Coffey CE, Cummings JL (eds): The American Psychiatric Publishing Textbook of Geriatric Neuropsychiatry, Third Edition. Copyright © 2011 American Psychiatric Association.
Electroconvulsive Therapy and Related Treatments
Recommended Readings
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Lisanby SH: Electroconvulsive therapy for depression. N Engl J Med
357:1939–1945, 2007
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